A new humanized mouse model for alopecia areata.

Although alopecia areata (AA) is not life threatening, it may lead to severe psychological disturbances, reducing the quality of life in all ages. Thus, a new animal model is needed for shedding more light onto the pathogenesis of this cell-mediated, organ-specific autoimmune disease to identify more effective therapeutic strategies. Recently, we succeeded in developing a new humanized mouse model of AA, which includes transplantation of healthy human scalp skin obtained from normal volunteers on to severe-combined immunodeficient mice.

The beneficial effect of blocking Kv1.3 in the psoriasiform SCID mouse model.

The Kv1.3 channel is important in the activation and function of effector memory T cells. Recently, specific blockers of the Kv1.

Lymphocytes, neuropeptides, and genes involved in alopecia areata.

Many lessons in autoimmunity - particularly relating to the role of immune privilege and the interplay between genetics and neuroimmunology - can be learned from the study of alopecia areata, the most common cause of inflammation-induced hair loss. Alopecia areata is now understood to represent an organ-restricted, T cell-mediated autoimmune disease of hair follicles. Disease induction is associated with collapse of hair follicle immune privilege in both humans and in animal models.